It has long been recognized that exposure to airborne particles is associated with increased morbidity and mortality in respiratory and cardiovascular health. See ref. 1 and 2. Particulate irritants are believed to induce pulmonary inflammation, cardiac autonomic function, endothelial dysfunction, systemic inflammation, oxidative stress, and altered balance between blood clotting and fibrinolysis. Larger particles have been considered to present less risk of irritation per unit mass due to higher surface area to volume ratios. See ref. 3-5. Airborne particulate matter associated with automobile exhaust has been indicated as particularly pernicious. See ref. 6-8.
Endothelial dysfunction (EdF) has been recognized as a strong predictor of adverse cardiovascular outcomes and is by now widely recognized as being, itself, a mechanism of increased cardiovascular risk. See ref. 9-12. Measurements of coronary microvascular function, which can be obtained non-invasively, provide a functional measure that relates to underlying endothelial function. Improvement of microvascular function is often reported as the goal and primary study endpoint for a variety of pharmaceutical intervention schemes. See e.g. ref 13-22.
Here we report that microvascular function can be improved in humans at cardiovascular risk by interventions directed at reducing exposure to airborne fine particles.